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Biomedical subjects

E M Ornitz

Publications and source records attributed to E M Ornitz.

At least 37 records · Page 2Linked to original sources

Startle modulation in children with posttraumatic stress disorder.

Startle responses to bursts of white noise were recorded as blink reflexes 17-21 months after a traumatic event in six children with posttraumatic stress disorder (PTSD) and in six normal control children. A seventh child with PTSD was studied on four occasions during the 2 years following a stressful event. The startle responses were modulated by nonstartling acoustic prestimulation in order to study the inhibitory and facilitatory modulation of startle reaction by brainstem mechanisms. The children with PTSD experienced a significant loss of the normal inhibitory modulation of startle response, suggesting that the traumatic experience had induced a long-lasting brainstem dysfunction.

Acoustic Stimulation↗

Synaptic connections of horizontal canal mediated ascending Deiters tract axons on medial rectus motoneurons in cat.

This study demonstrates the termination of ascending tract of Deiters' (ATD) axons on ipsilateral medial rectus (MR) motoneurons. Horseradish peroxidase (HRP) was iontophoretically injected into ATD axons which were recorded in the MR motoneuron pool of the oculomotor nucleus. MR motoneuron cell bodies were identified by retrograde transport of HRP injected into MR muscles in the orbit. ATD axons were identified by Type I responses to horizontal rotation, monosynaptic responses on stimulation of the ipsilateral labyrinth, and no response on contralateral labyrinth or contralateral abducens nucleus or on ipsilateral MR nerve stimulation. Light microscopic examination showed the main stem axons to be lateral to the medial longitudinal fasciculus, and terminal boutons were in contact with ipsilateral identified MR motoneurons (Furuya and Markham: Exp. Brain Res. 43: 289-303, 1981). Light microscopy and semi-thin sections showed boutons of ATD in contact with identified MR motoneuron cell bodies and proximal dendrites. The electron micrographs (EM) showed the HRP-injected ATD axons have synapses on MR motoneurons. ATD boutons made axosomatic and axodendritic synapses on MR motoneurons. The boutons contained numerous spheroidal synaptic vesicles. Several examples showed clear asymmetrical post-synaptic membrane specialization. This confirms the synaptic connection between horizontal canal activated elements in the ATD and MR motoneurons.

Abducens Nerve↗

Brain-stem dysfunction in autism. Results of vestibular stimulation.

Responses to vestibular stimulation can, under well-controlled experimental conditions, provide a measure of brain-stem function. Autistic children had significantly longer time constants during the primary nystagmus response and significantly fewer beats during the secondary response than normal children when stimulated with constant angular acceleration in complete darkness. These findings could not be attributed to gross differences in arousal, to developmental retardation, to associated clinical conditions, or to either the influence of vision or habituation. Rather, they are suggestive of a neurophysiologic dysfunction, perhaps involving the brain stem, and may be an expression of the process that underlies those autistic behaviors that suggest faulty modulation of sensory input and motor output. Brain-stem centers modulate both general sensory input and motor excitation and may play a role in the elaboration of the more complex adaptive and motivated behaviors that are also disturbed in autism.

Arousal↗

Autistic children who become schizophrenic.

Infantile autism and schizophrenia have been regarded as unrelated and distinct disorders. There is, however, some evidence in the literature that supports a relationship between the two disorders in that there may be a subgroup of autistic children in whom schizophrenia develops. The diagnostic criteria used in the literature to describe infantile autism and schizophrenia in childhood has not been uniform. The three cases in this report, diagnosed on the basis of current criteria and detailed clinical descriptions, clearly point to an initial diagnosis of infantile autism followed by the development of schizophrenia.

Adolescent↗

The functional neuroanatomy of infantile autism.

Infantile autism is a behavioral syndrome consisting of specific disturbances of social relating and communication, language, response to objects, sensory sensitivity and motility. The uniqueness of this syndrome suggests one underlying pathophysiologic mechanism, although multiple etiologies, which could activate or replicate such a mechanism, have been demonstrated. Review of considerable experimental evidence and clinical observation suggests that the symptomatology of autism, including the disturbances of social relating and communication, can best be explained as a disorder of sensory modulation. This in turn suggests a neurophysiologic mechanism consisting of dysfunction of a cascading series of neurophysiologic levels or interacting neuronal loops in the brainstem and diencephalon which subserve modulation of sensory input. Some of those same systems modulate motor output in response to sensory input, and their dysfunction may release the abnormal perseverative motility of infantile autism. Other experimental evidence and clinical observations stress the language deficits of autism and implicate dysfunction of cortical structures. Brainstem and diencephalic centers project rostrally to telencephalic structures and these, in turn, modify brainstem and diencephalic function. Theories of rostrally and caudally directed sequences of pathoneurophysiologic contributions to the system dysfunction in autism are compared. It is concluded that the symptoms of autism can best be explained in terms of dysfunction of brainstem and related diencephalic behavioral systems and their elaboration and refinement by selected higher neural structures.

Arousal↗

Influence of click sound pressure direction on brain stem responses in children.

Brain stem auditory responses were evoked by stimulation with condensation (C) and rarefaction (R) clicks separately. The latencies of the first five waves of the response were compared in response to the two sound pressure directions. Responses to R clicks were significantly shorter than responses to C clicks for wave 4, in the absence of consistent response differences in the other waves.

Acoustic Stimulation↗

The maturation of vestibular nystagmus in infancy and childhood.

The displacements, durations, and velocities of the slow and fast components of both the primary and secondary nystagmus induced by constant angular acceleration were measured in 46 normal children 1 month to 11 years old. There were significant changes in nystagmus parameters in respect to maturation. The young infant had larger amplitude, higher velocity beats than the older child during both the primary and the secondary nystagmus. Parameters describing both the primary and the secondary nystagmus reached their peak values and terminated earlier in the infant than in the older child. Although the slow component velocity during secondary nystagmus was much slower than during the primary nystagmus at all ages, the secondary nystagmus/primary nystagmus ratio was significantly greater in early infancy. Thus, in infancy, as compared with later childhood, the vigor of the secondary nystagmus was disproportionately greater than the primary nystagmus. These results were discussed in relation to the maturation both of vestibular responsiveness and of vestibular adaptation.

Age Factors↗

The early development of autistic children.

A sample of 74 young autistic children was selected and defined by direct observation of specific behaviors and clinical assessment of the presence or absence of associated pathological conditions. Retrospective developmental data on these children and 38 age-matched normal children were gathered by means of a written inventory completed by the parents when the children were relatively young (mean age less than 4 years). The autistic children were reported to have had significant delays in the development of motor abilities, speech, communication, comprehension, and, to a lesser extent, perception during their 1st and 2nd years.

Age Factors↗

Rapid eye movement (REM) activity in normal and autistic children during REM sleep.

Thirty normal children (aged 3--68 months) and 16 autistic children (aged 36--62 months) were recorded during nonmedicated sleep and data pertaining to rapid eye movements (REM) were measured during the first three REM periods of the night. When time of night from which data were gathered was held constant, normal children showed a significant relationship between age and the organization of eye movements into discrete bursts. When autistic children were compared to age-matched normal controls, they showed an immaturity in this phenomena, their results being similar to those found in children less than 18 months of age. Such an immaturity could result from dysfunction at a number of diverse levels and sites in the central nervous system.

Age Factors↗

The syndrome of autism: a critical review.

The authors review the clinical features and behavioral characteristics of autism; differential diagnosis of the syndrome; clinical, neurophysiological, and biochemical research; and its medical management and treatment. They conclude that autism is a behaviorally defined, specific syndrome that is manifested at birth or shortly thereafter. Its symptoms are expressive of an underlying neuropathophysiological process that affects developmental rate; modulation of perception; language, cognitive, and intellectual development; and the ability to relate. The long-term prognosis is guarded; almost all patients manifest severe symptomatology throughout their lives. Further basic research into the neuropathophysiological process underlying the syndrome is necessary in order to reach the ultimate goal of developing etiologically specific treatment programs.

Age Factors↗

Evolution of sleep spindles in childhood.

Twenty-six normal children (age range range 4-68 months) were studied during Stage 2 sleep which occurred within 20 min preceding or following the first three REM periods of the night. Sleep spindles were measured in Fp1T3. The number, length, and percent of sleep spindle activity were found to be maximal at 46 months of age. Beyond 6 months spindle activity decreased to reach minimal values by 27 months, remained fairly constant to 54 months, then rose again to higher values in the oldest subjects. The mean spindle-wave frequency was 1314 c/sec in subjects younger than 40 months, but was 12-13 c/sec in older subjects. Spindle onsets in Fp1T3 and Fp2T4 were more often concurrent in older as compared to younger subjects. Auditory stimulation (binaural clicks, 60 dB above hearing threshold) affected neither the incidence nor the length of spindles during sleep. Because sizable changes in sleep spindle activity are found between 3 months and 5 years of age, and because such changes are relatively consistent between subjects, it is concluded that sleep spindles recorded between frontal and temporal areas may serve as a useful index of neural maturation in the human subject.

Acoustic Stimulation↗